Abstract
Pancreatic β-cell failure on a background of insulin resistance results in the inability to compensate for fasting hyperglycaemia and eventually produces type 2 diabetes mellitus. We describe an interesting case of a patient who presented acutely with unprovoked severe hyperglycaemic hyperosmolar state and was subsequently diagnosed with type 2 diabetes mellitus on a background of only impaired first phase insulin secretion 4 months prior. Glucagon stimulation test detected significant β-cell failure necessitating long term exogenous insulin therapy which is highly unusual by virtue of the rapid apparent deterioration.
Highlights
Type 2 Diabetes Mellitus (T2DM) is undoubtedly the scourge of the developed world and a source of considerable socioeconomic burden [1]
We describe an interesting case of a patient who presented acutely with unprovoked severe hyperglycaemic hyperosmolar state and was subsequently diagnosed with type 2 diabetes mellitus on a background of only impaired first phase insulin secretion 4 months prior
The exact aetiology of T2DM remains unknown, it involves a combination of insulin resistance and some degree of pre-existing b-cell secretory dysfunction conferring a state of relative rather than absolute insulin deficiency which progressively deteriorates with time irrespective of treatment [2,3,4,5]
Summary
Type 2 Diabetes Mellitus (T2DM) is undoubtedly the scourge of the developed world and a source of considerable socioeconomic burden [1]. Other than clinical features of dehydration and mild central abdominal adiposity with a waist: hip ratio of 1.04, there were no other significant clinical signs His random plasma glucose (RPG) on arrival was 59.1 mmol/L. There was no history of specific weight loss over the preceding months His general practitioner (GP) had performed a fasting plasma glucose test on him in February 2008 which showed a value of 6.4 mmol/L. Subsequent 75 gram (g) oral glucose tolerance test (OGTT) produced a value of 15.3 mmol/L, 14.1 mmol/L and 7.6 mmol/L 30 minutes, 1-hour and 2-hours post glucose load respectively He was managed with dietary modification and exercise. His acute presentation was consistent with hyperglycaemic hyperosmolar state (HHS) and acute renal failure secondary to dehydration He was treated with intravenous insulin and intensively rehydrated with close attention to electrolyte balance. His average capillary blood glucose (CBG) was 6.7 mmol/L and range 6.5-7.7 mmol/L on discharge
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